Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2025
Exploring the chemotherapeutic potential of diosmetin ruthenium-p-cymene complex in bladder cancer treatment through the regulation of the PI3K/β-catenin/TJP1/AR signaling pathway.
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Sil Sidhanta, Gayen Sakuntala, Seal Ishita, Das Abhijit, Roy Souvik
Аннотация
BACKGROUND: Bladder cancer is the deadliest cause of cancer-related morbidity worldwide. The metal-flavonoid compound, diosmetin ruthenium-p-cymene complex, demonstrated a remarkable toxicological profile in different toxicological and genotoxicological studies. In this context, the study aimed to explore the chemotherapeutic effects of the diosmetin ruthenium-p-cymene complex in bladder cancer treatment through in vitro and in vivo approaches.
METHODS: The in vitro assessment was carried out through cell viability assay, apoptotic assay by flow cytometry, and western blot study on both T24 and RT4 cells. Subsequently, the anticancer activity of the complex was assessed by BBN-induced bladder cancer in rats.
RESULTS: As a result, the downregulation of TJP1, AR, and β-catenin expression with upregulation of PTEN expression was evaluated by western blot analysis. Cell cycle arrest was occurred and depicted via flow cytometric analysis. In the in-vivo study, the complex treatment significantly restored the normal bladder architecture. The induction of apoptotic events via downregulation of β-catenin, PI3K, Akt, and mTOR expression and upregulation of PTEN expression, showed in immunohistochemical analysis.
CONCLUSION: Consequently, the treatment with complex represented a promising chemotherapeutic activity by the modulation of tumor microenvironment through altering PI3K/ β-catenin/TJP1/AR facilitated signaling pathway involved with apoptosis induction in bladder carcinoma.
METHODS: The in vitro assessment was carried out through cell viability assay, apoptotic assay by flow cytometry, and western blot study on both T24 and RT4 cells. Subsequently, the anticancer activity of the complex was assessed by BBN-induced bladder cancer in rats.
RESULTS: As a result, the downregulation of TJP1, AR, and β-catenin expression with upregulation of PTEN expression was evaluated by western blot analysis. Cell cycle arrest was occurred and depicted via flow cytometric analysis. In the in-vivo study, the complex treatment significantly restored the normal bladder architecture. The induction of apoptotic events via downregulation of β-catenin, PI3K, Akt, and mTOR expression and upregulation of PTEN expression, showed in immunohistochemical analysis.
CONCLUSION: Consequently, the treatment with complex represented a promising chemotherapeutic activity by the modulation of tumor microenvironment through altering PI3K/ β-catenin/TJP1/AR facilitated signaling pathway involved with apoptosis induction in bladder carcinoma.